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in mosquito gut
Image by Antoine Nicot
and Jacques Denoyelle
Parasites that develop resistance to the antimalarial drug atovaquone cannot pass this resistance on to their offspring, a new study suggests.
Researchers found that malaria parasites develop resistance to atovaquone via mutations in the mitochondrial cytochrome b complex.
However, these mutations also prevent female parasites from reproducing, so the resistance cannot be passed on to future generations.
Geoff McFadden, PhD, of the University of Melbourne in Victoria, Australia, and his colleagues reported these findings in Science.
“These results are very exciting because the spread of drug resistance is currently destroying our ability to control malaria,” Dr McFadden said.
“We now understand the particular genetic mutation that gave rise to drug resistance in some malaria parasite populations and how it eventually kills them in the mosquito, providing new targets for the development of drugs. So the development of drug resistance may not be a major problem if the resistance cannot spread, meaning the drug atovaquone could be more widely used in malaria control.”
To conduct this study, Dr McFadden and his colleagues analyzed 3 atovaquone-resistant strains of Plasmodium berghei, a malaria parasite that infects rodents. Each strain contained a different mutation in cytochrome b.
The researchers found that 2 of the mutations resulted in developmental defects in the parasite zygotes, and the third mutation resulted in complete infertility in the parasites due to severely impaired female germ cells.
Cross breeding parasites with and without these mutations showed that the mutations are not passed on to offspring. From 44 separate transmission attempts involving 750 mosquito bites, transmission of atovaquone resistance was only observed once, and this mutant was unable to transmit further, despite 7 attempts.
The researchers said it appears that atovaquone-resistant mutations severely impair the lifecycle of the parasites when they are living in mosquito hosts, so these mutations cannot be passed on.
In the human malaria parasite Plasmodium falciparum, the researchers identified similar mutations that impaired the ability of the parasites to infect mosquitos, as well as the number of oocysts produced when infection did occur. 
in mosquito gut
Image by Antoine Nicot
and Jacques Denoyelle
Parasites that develop resistance to the antimalarial drug atovaquone cannot pass this resistance on to their offspring, a new study suggests.
Researchers found that malaria parasites develop resistance to atovaquone via mutations in the mitochondrial cytochrome b complex.
However, these mutations also prevent female parasites from reproducing, so the resistance cannot be passed on to future generations.
Geoff McFadden, PhD, of the University of Melbourne in Victoria, Australia, and his colleagues reported these findings in Science.
“These results are very exciting because the spread of drug resistance is currently destroying our ability to control malaria,” Dr McFadden said.
“We now understand the particular genetic mutation that gave rise to drug resistance in some malaria parasite populations and how it eventually kills them in the mosquito, providing new targets for the development of drugs. So the development of drug resistance may not be a major problem if the resistance cannot spread, meaning the drug atovaquone could be more widely used in malaria control.”
To conduct this study, Dr McFadden and his colleagues analyzed 3 atovaquone-resistant strains of Plasmodium berghei, a malaria parasite that infects rodents. Each strain contained a different mutation in cytochrome b.
The researchers found that 2 of the mutations resulted in developmental defects in the parasite zygotes, and the third mutation resulted in complete infertility in the parasites due to severely impaired female germ cells.
Cross breeding parasites with and without these mutations showed that the mutations are not passed on to offspring. From 44 separate transmission attempts involving 750 mosquito bites, transmission of atovaquone resistance was only observed once, and this mutant was unable to transmit further, despite 7 attempts.
The researchers said it appears that atovaquone-resistant mutations severely impair the lifecycle of the parasites when they are living in mosquito hosts, so these mutations cannot be passed on.
In the human malaria parasite Plasmodium falciparum, the researchers identified similar mutations that impaired the ability of the parasites to infect mosquitos, as well as the number of oocysts produced when infection did occur.
in mosquito gut
Image by Antoine Nicot
and Jacques Denoyelle
Parasites that develop resistance to the antimalarial drug atovaquone cannot pass this resistance on to their offspring, a new study suggests.
Researchers found that malaria parasites develop resistance to atovaquone via mutations in the mitochondrial cytochrome b complex.
However, these mutations also prevent female parasites from reproducing, so the resistance cannot be passed on to future generations.
Geoff McFadden, PhD, of the University of Melbourne in Victoria, Australia, and his colleagues reported these findings in Science.
“These results are very exciting because the spread of drug resistance is currently destroying our ability to control malaria,” Dr McFadden said.
“We now understand the particular genetic mutation that gave rise to drug resistance in some malaria parasite populations and how it eventually kills them in the mosquito, providing new targets for the development of drugs. So the development of drug resistance may not be a major problem if the resistance cannot spread, meaning the drug atovaquone could be more widely used in malaria control.”
To conduct this study, Dr McFadden and his colleagues analyzed 3 atovaquone-resistant strains of Plasmodium berghei, a malaria parasite that infects rodents. Each strain contained a different mutation in cytochrome b.
The researchers found that 2 of the mutations resulted in developmental defects in the parasite zygotes, and the third mutation resulted in complete infertility in the parasites due to severely impaired female germ cells.
Cross breeding parasites with and without these mutations showed that the mutations are not passed on to offspring. From 44 separate transmission attempts involving 750 mosquito bites, transmission of atovaquone resistance was only observed once, and this mutant was unable to transmit further, despite 7 attempts.
The researchers said it appears that atovaquone-resistant mutations severely impair the lifecycle of the parasites when they are living in mosquito hosts, so these mutations cannot be passed on.
In the human malaria parasite Plasmodium falciparum, the researchers identified similar mutations that impaired the ability of the parasites to infect mosquitos, as well as the number of oocysts produced when infection did occur.